Table 1.
ImmR inhibits acquisition of ICEBs1 by recipient cells and is bypassed by expression of int.
| Recipienta (strain No.) | Mating frequencyb |
|---|---|
| 1. ICEBs10 (CAL419) | (5.1 ± 2.4) × 10−3 |
| 2. ICEBs1+ (JMA875) | (9.2 ± 4.0) × 10−6 |
| 3. ICEBs10; PimmR-immR (JMA872) | (2.4 ± 0.62) × 10−6 |
| 4. ICEBs10; PimmR-immR; Pspank-int (JMA873) | (2.0 ± 0.84) × 10−3 |
| 5. ICEBs10; Pspank-int (JMA878) | (8.0 ± 2.3) × 10−3 |
| 6. ICEBs1(Δint); Pspank-int (JMA882) | (2.2 ± 0.78) × 10−4 |
a
All recipients contained a comK null mutation and were streptomycin resistant (str). Recipient cells containing Pspank-int were grown in the presence of IPTG to allow production of Int.
b
Mating assays were performed as described (Auchtung et al., 2005). The mating frequency is the mean number of transconjugants per donor cell (±standard error of the mean), calculated from at least two experiments. The donor strain was JMA168 [ICEBs1(ΔrapIphrI∷kan); Pspank(hy)-rapI]. Expression of Pspank(hy)-rapI was induced with IPTG 1 h before mating. Production of RapI causes excision of ICEBs1 and expression of its conjugation genes.